BACKGROUND/AIMS: Povidone-iodine (PI) is commonly used as a preoperative disinfectant; however, it has been shown to be cytotoxic. The present study was performed to investigate the mechanism by which PI causes cell death. METHODS: Primary human corneal fibroblasts (HCF) and a human corneal epithelial cell line (HCEC) were treated with 0.1-5% PI for 1 min. Cell morphology and growth were examined by phase-contrast microscopy and genomic DNA quantification. Cellular enzyme activities were detected by water-soluble tetrazolium salt (WST-1) and calcein-acetoxymethylester staining, whereas membrane integrity was determined by a membrane-impermeable dye. The cell fixation effect of PI was assayed by analysis of genomic DNA integrity and resistance to ionic detergent SDS lysis. The interleukin-8 (IL-8) secretion after adding interleukin-1ß (IL-1b) or lipopolysaccharide (LPS) was determined by ELISA. RESULTS: PI treatment inhibited HCF and HCEC cell growth without changing cellular morphology; however, cells became resistant to SDS lysis. The mitochondrial dehydrogenase and intracellular esterase activities as well as cell membrane integrity were abolished by PI treatment. Genomic DNA integrity from PI-treated groups was similar to that from alcohol-fixed groups. IL-1b- and LPS-induced IL-8 secretion was abolished by PI treatment. CONCLUSIONS: Where PI concentration is sufficient to cause cell death, this occurs through fixation rather than necrosis in cultured human corneal stromal and epithelial cell.
BACKGROUND/AIMS: Povidone-iodine (PI) is commonly used as a preoperative disinfectant; however, it has been shown to be cytotoxic. The present study was performed to investigate the mechanism by which PI causes cell death. METHODS: Primary human corneal fibroblasts (HCF) and a human corneal epithelial cell line (HCEC) were treated with 0.1-5% PI for 1 min. Cell morphology and growth were examined by phase-contrast microscopy and genomic DNA quantification. Cellular enzyme activities were detected by water-soluble tetrazolium salt (WST-1) and calcein-acetoxymethylester staining, whereas membrane integrity was determined by a membrane-impermeable dye. The cell fixation effect of PI was assayed by analysis of genomic DNA integrity and resistance to ionic detergent SDS lysis. The interleukin-8 (IL-8) secretion after adding interleukin-1ß (IL-1b) or lipopolysaccharide (LPS) was determined by ELISA. RESULTS: PI treatment inhibited HCF and HCEC cell growth without changing cellular morphology; however, cells became resistant to SDS lysis. The mitochondrial dehydrogenase and intracellular esterase activities as well as cell membrane integrity were abolished by PI treatment. Genomic DNA integrity from PI-treated groups was similar to that from alcohol-fixed groups. IL-1b- and LPS-induced IL-8 secretion was abolished by PI treatment. CONCLUSIONS: Where PI concentration is sufficient to cause cell death, this occurs through fixation rather than necrosis in cultured human corneal stromal and epithelial cell.
Authors: Laura Ortega-Llamas; María I Quiñones-Vico; Marta García-Valdivia; Ana Fernández-González; Ana Ubago-Rodríguez; Raquel Sanabria-de la Torre; Salvador Arias-Santiago Journal: Cells Date: 2022-04-20 Impact factor: 7.666
Authors: Hyun-Sung Lee; Hee-Jin Jang; Eric M Lo; Cynthia Y Truong; Shawn S Groth; Joseph S Friedberg; David J Sugarbaker; Bryan M Burt Journal: Interact Cardiovasc Thorac Surg Date: 2019-03-01
Authors: Diane T Siegel; G Baker Hubbard; Jiong Yan; Blaine Cribbs; Nieraj Jain; Steve Yeh; Diem Bui; Jesse Smith; Scott Barb; William Pearce; Laura Ward; Andrew M Hendrick Journal: Retina Date: 2020-08 Impact factor: 3.975